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CorrectionErratum

Correction to “Rimonabant, a Cannabinoid Receptor Type 1 Inverse Agonist, Inhibits Hepatocyte Lipogenesis by Activating Liver Kinase B1 and AMP-Activated Protein Kinase Axis Downstream of Gαi/o Inhibition”

Molecular Pharmacology September 2012, 82 (3) 561-562; DOI: https://doi.org/10.1124/mol.82.3.561
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  • Fig. 4.
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    Fig. 4.

    A, effect of PKA on serine phosphorylation of LXRα by rimonabant. HepG2 cells were treated with vehicle or 10 μM rimonabant after siPKA transfection (100 pmol/ml) for 48 h or 1 μM H89 treatment for 1 h. LXRα immunoprecipitates (IP) were immunoblotted (IB) with anti-phosphorylated serine antibody (pSer). After verifying equal loading of proteins in each experiment by immunoblotting of LXRα immunoprecipitates for LXRα, the relative protein levels of pSer-LXRα from at least three separate experiments were compared among four treatment groups in each experimental set (i.e., siCON + vehicle, siCON + rimonabant, siPKA + vehicle, and siPKA + rimonabant, or vehicle, vehicle + rimonabant, H89 + vehicle, and H89 + rimonabant) by analysis of variance and multiple comparisons (**, p < 0.01; compared from siCON + vehicle or vehicle-treated group). Left LXRα control blot is also the control blot for pThr-LXRα (Fig 6D, right). WCL, whole cell lysate. (Legend continues as in original.)

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    Fig. 6.

    (Legend begins as in original.) D, effect of DN-AMPK transfection or PKA knockdown (100 pmol/ml, 48 h) on LXRα phosphorylation by rimonabant. LXRα immunoprecipitates (IP) were immunoblotted (IB) with anti-phosphorylated threonine (pThr) or anti-phosphorylated serine (pSer) antibody. The LXRα control blot shown in D, left, is for pSer-LXRα (D, middle). The LXRα control blot shown in Fig. 4A, left, is for pThr-LXRα (D, right). Immunoblots for c-myc confirmed DN-AMPK overexpression. After verifying equal loading of proteins in each experiment by immunoblotting of LXRα immunoprecipitates for LXRα, the relative protein levels of pSer-LXRα or pThr-LXRα from at least three separate experiments were compared among four treatment groups in each experimental set (i.e., MOCK + vehicle, MOCK + rimonabant, DN-AMPK + vehicle, and DN-AMPK + rimonabant; or siCON + vehicle, siCON + rimonabant, siPKA + vehicle, and siPKA + rimonabant) by analysis of variance and multiple comparisons.

  • Fig. 6A.
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    Fig. 6A.

    A, AMPK activation by rimonabant (Rimo).

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Molecular Pharmacology: 82 (3)
Molecular Pharmacology
Vol. 82, Issue 3
1 Sep 2012
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CorrectionErratum

Correction to “Rimonabant, a Cannabinoid Receptor Type 1 Inverse Agonist, Inhibits Hepatocyte Lipogenesis by Activating Liver Kinase B1 and AMP-Activated Protein Kinase Axis Downstream of Gαi/o Inhibition”

Molecular Pharmacology September 1, 2012, 82 (3) 561-562; DOI: https://doi.org/10.1124/mol.82.3.561

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CorrectionErratum

Correction to “Rimonabant, a Cannabinoid Receptor Type 1 Inverse Agonist, Inhibits Hepatocyte Lipogenesis by Activating Liver Kinase B1 and AMP-Activated Protein Kinase Axis Downstream of Gαi/o Inhibition”

Molecular Pharmacology September 1, 2012, 82 (3) 561-562; DOI: https://doi.org/10.1124/mol.82.3.561
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